Sleep Disorders: Sleep Disorders III |

Intermittent Hypoxia Reduces Microglia Proliferation and Induces DNA Damage In Vitro FREE TO VIEW

Song Liu, MD; Zhonghua Wang; Bo Xu; Kui Chen; Lianping Ren, MS; Jinyuan Sun
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Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China

Copyright 2016, American College of Chest Physicians. All Rights Reserved.

Chest. 2016;149(4_S):A577. doi:10.1016/j.chest.2016.02.602
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SESSION TITLE: Sleep Disorders III

SESSION TYPE: Original Investigation Poster

PRESENTED ON: Saturday, April 16, 2016 at 11:45 AM - 12:45 PM

PURPOSE: Obstructive sleep apnea (OSA) is a common sleep disorder characterized by recurrent episodes of complete or partial collapse of the upper airway, resulting in nocturnal intermittent hypoxia (IH). This disease has many potential consequences including neurocognitive and behavioral deficits. IH, caused by OSA, could cause hippocampus or neuron damage through multiple signaling pathways, while the underlying mechanisms are still unclear. The effect of IH on the growth and biological functions of microglia cells was explored.

METHODS: Cell proliferation of BV2 cells after exposure to IH were observed by MTT assay and then DNA damage was detected by comet assay. Afterwards, RNA-sequencing assay was performed in cells under IH condition and normal conditions as control to find out the potential differentially expressed genes, which were further confirmed by Reverse Transcriptase Polymerase Chain Reaction (RT-PCR) and Western blot assay. Moreover, inflammation factors were detected in BV2 cells under IH condition.

RESULTS: IH inhibited the proliferation of BV2 cells, as well as caused DNA damage. RNA-sequencing assay revealed 4 differentially expressed genes which were associated with the network of P53 signaling pathways in BV2 cells. IH inhibited cyclinD1 and cyclinE2 expression via initiating multiple P53 pathways, which further blocked cell cycle transition and attenuated the proliferative capability of BV2 cells.

CONCLUSIONS: IH reduces microglia proliferation and induces DNA damage by activated inflammation reactions.

CLINICAL IMPLICATIONS: Neurocognitive deficits of patients with OSA may relate to the nerve inflammation induced by IH, and that p53 induced the expression of CyclinD1 and cyclinE2 play a certain role in the neuroinflammation.

DISCLOSURE: The following authors have nothing to disclose: Song Liu, Zhonghua Wang, Bo Xu, Kui Chen, Lianping Ren, Jinyuan Sun

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